Glutaminostatin: Another facet of glucagon as a regulator of plasma amino acid concentrations

Hayashi, Yoshitaka

doi:10.1111/jdi.13110

Cited by 8 publications

(8 citation statements)

References 9 publications

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“…Amino acids stimulate α‐cell glucagon secretion and cellular proliferation, whereas glucagon enhances amino acid metabolism in the liver 3,4 . Thus, our clinical result could clinically validate the correlation between glucagon and amino acids found by basic glucagon studies 18 . From these findings, I propose a new concept of diabetes as a “comprehensive nutrition disorder”, caused by both insulin and glucagon dysregulation (Figure 1, see legend for details).…”

Section: Figuresupporting

confidence: 72%

Beginning of a new era in glucagon research: Breakthrough by the new glucagon assay

Kawamori

2020

J of Diabetes Invest

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Section: Figuresupporting

confidence: 72%

Beginning of a new era in glucagon research: Breakthrough by the new glucagon assay

Kawamori

2020

J of Diabetes Invest

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“…Glucagon plays an essential role in the homeostatic regulation of amino acids 5 , 13 , 14 , and an intake of amino acids (proteins) resulted in a strong stimulation of pancreatic α‐cells to secrete glucagon 15 . As protein‐derived calories account for approximately 15% of the total caloric intake in the modern diet 16 , a mixed meal tolerance test (MMTT) 17 is suitable rather than an oral glucose tolerance test when evaluating the influence of glucagon abnormality on glycemic control in the daily lives of diabetes patients.…”

Section: Introductionmentioning

confidence: 99%

Impact of glucagon response on early postprandial glucose excursions irrespective of residual β‐cell function in type 1 diabetes: A cross‐sectional study using a mixed meal tolerance test

Ito

Horie

Miwa

et al. 2021

J of Diabetes Invest

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Aims/Introduction Controlling postprandial glucose levels in patients with type 1 diabetes is challenging even under the adequate treatment of insulin injection. Recent studies showed that dysregulated glucagon secretion exacerbates hyperglycemia in type 2 diabetes patients, but little is known in type 1 diabetes patients. We investigated whether the glucagon response to a meal ingestion could influence the postprandial glucose excursion in patients with type 1 diabetes. Materials and Methods We enrolled 34 patients with type 1 diabetes and 23 patients with type 2 diabetes as controls. All patients underwent a liquid mixed meal tolerance test. We measured levels of plasma glucose, C‐peptide and glucagon at fasting (0 min), and 30, 60 and 120 min after meal ingestion. All type 1 diabetes patients received their usual basal insulin and two‐thirds of the necessary dose of the premeal bolus insulin. Results The levels of plasma glucagon were elevated and peaked 30 min after the mixed meal ingestion in both type 1 diabetes and type 2 diabetes patients. The glucagon increments from fasting to each time point (30, 60 and 120 min) in type 1 diabetes patients were comparable to those in type 2 diabetes patients. Among the type 1 diabetes patients, the glucagon response showed no differences between the subgroups based on diabetes duration (<5 vs ≥5 years) and fasting C‐peptide levels (<0.10 vs ≥0.10 nmol/L). The changes in plasma glucose from fasting to 30 min were positively correlated with those in glucagon, but not C‐peptide, irrespective of diabetes duration and fasting C‐peptide levels in patients with type 1 diabetes. Conclusions The dysregulated glucagon likely contributes to postprandial hyperglycemia independent of the residual β‐cell functions during the progression of type 1 diabetes.

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“…Although GLP-1 and glucagon are formed from a common precursor (Hayashi, 2019), glucagon levels did not change among the study groups.…”

Section: Association Of Ghrelin With Incretinsmentioning

confidence: 76%

The Links of Ghrelin to Incretins, Insulin, Glucagon, and Leptin After Bariatric Surgery

et al. 2021

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Type 2 diabetes mellitus (T2DM) is one of the most prominent and socially significant problems. The present study aimed to identify the mechanisms of interaction of critical regulators of carbohydrate metabolism using bioinformatics and experimental methods and to assess their influence on the development of T2DM. We conducted an in silico search for the relationship of hormones and adipokines and performed functional annotation of the receptors for ghrelin and incretins. Hormones and adipokines were assessed in the plasma of obese patients with and without T2DM as well as after laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (RYGB) surgeries. Incretin- and ghrelin-associated functions and metabolic processes were discovered. Low ghrelin levels were observed in obese patients without T2DM compared with healthy volunteers and the other groups. The highest ghrelin levels were observed in obese patients with T2DM. This defense mechanism against insulin resistance could be realized through the receptors G-protein-coupled receptor (GPCR), growth hormone secretagogue receptor (GHSR), and growth hormone-releasing hormone receptor (GHRHR). These receptors are associated with proliferative, inflammatory, and neurohumoral signaling pathways and regulate responses to nutrient intake. Signaling through the GPCR class unites ghrelin, glucagon, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide (GLP)-1. Ghrelin impairs carbohydrate and lipid metabolism in obese patients. Ghrelin is associated with elevated plasma levels of insulin, glucagon, and leptin. Specific activation of receptors and modulation by posttranslational modifications of ghrelin can control IR’s development in obesity, which is a promising area for research.

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Glutaminostatin: Another facet of glucagon as a regulator of plasma amino acid concentrations

Cited by 8 publications

References 9 publications

Beginning of a new era in glucagon research: Breakthrough by the new glucagon assay

Beginning of a new era in glucagon research: Breakthrough by the new glucagon assay

Impact of glucagon response on early postprandial glucose excursions irrespective of residual β‐cell function in type 1 diabetes: A cross‐sectional study using a mixed meal tolerance test

The Links of Ghrelin to Incretins, Insulin, Glucagon, and Leptin After Bariatric Surgery

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